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NK T cell activation promotes Chlamydia trachomatis infection in vivo.

Authors
  • Bilenki, Laura1
  • Wang, Shuhe
  • Yang, Jie
  • Fan, Yijun
  • Joyee, Antony George
  • Yang, Xi
  • 1 Laboratory for Infection and Immunity, Department of Immunology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada. , (Canada)
Type
Published Article
Journal
Journal of immunology (Baltimore, Md. : 1950)
Publication Date
Sep 01, 2005
Volume
175
Issue
5
Pages
3197–3206
Identifiers
PMID: 16116210
Source
Medline
License
Unknown

Abstract

We used two approaches to examine the role of NK T cells (NKT) in an intracellular bacterial (Chlamydia trachomatis mouse pneumonitis (C. muridarum)) infection. One is to use CD1 gene knockout (KO) mice, which lack NKT, and the other is to activate NKT using alpha-galactosylceramide (alpha-GalCer), a natural ligand of these cells. The data showed a promoting effect of NKT activation on Chlamydia lung infection. Specifically, CD1 KO mice exhibited significantly lower levels of body weight loss, less severe pathological change and lower chlamydial in vivo growth than wild-type mice. Immunological analysis showed that CD1 KO mice exhibited significantly lower C. muridarum-specific IL-4 and serum IgE Ab responses as well as more pronounced delayed-type hypersensitivity response compared with wild-type controls. In line with the finding in KO mice, the in vivo stimulation of NKT using alpha-GalCer enhanced chlamydial growth in vivo, which were correlated with reduced delayed-type hypersensitivity response and increased C. muridarum-driven IL-4/IgE production. Moreover, neutralization of IL-4 activity in the alpha-GalCer-treated BALB/c mice significantly reduced the promoting effect of alpha-GalCer treatment on chlamydial growth in vivo. These data provide in vivo evidence for the involvement of NKT in a bacterial pathogenesis and its role in promoting Th2 responses during infection.

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